Effects of trichostatin A on human lung cancer cell strains A549.
- Author:
Dong ZHANG
1
;
Chang-ting LIU
;
Xiao-dan YU
;
Yan LIU
Author Information
- Publication Type:Journal Article
- MeSH: Adenocarcinoma; metabolism; pathology; Apoptosis; drug effects; Cell Cycle; drug effects; Cell Line, Tumor; Extracellular Signal-Regulated MAP Kinases; metabolism; Histone Deacetylase Inhibitors; pharmacology; Humans; Hydroxamic Acids; pharmacology; Lung Neoplasms; metabolism; pathology
- From: Acta Academiae Medicinae Sinicae 2010;32(2):167-170
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effect of trichostatin A (TSA) on human lung cancer cell strains A549.
METHODSA549 cells were exposed to TSA at different concentrations, then the growth-inhibiting effects of the cell line were detected with 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay; After the cells were exposed to TSA for 48 and 96 hours at 300 nmol/L, the change of the cell cycle and apoptosis of A549 were analyzed with flow cytometry. p21 protein and extracellular signal regulated kinase (ERK) expression were detected by Western blot.
RESULTSTSA inhibited the growth of A549 cells in time- and concentration-dependent manners. The proportion of apoptosis, G0/G1 and G2/M phase increased in accordance with raising of the TSA concentration. The expression of p21 protein was significantly up-regulated and the expression of phosphorylation ERK was significantly down-regulated after A549 cells were treated with TSA.
CONCLUSIONSHistone deacetylase inhibitor TSA can inhibit the proliferation of human lung cancer cell strains A549 and induce the cell cycle arrest and apoptosis in the A549 cells. This may be related to up-regulation of p21 protein expression and the down-regulation of phosphorylation ERK.
